The revelation could pave the way for understanding the alterations of the intestinal system in diabetic patients
Analyzing the inflammatory profile of 54 patients who underwent biopsy, it was shown that those with type 1 diabetes show, at the intestinal mucosa level, a specific inflammatory state, "different" from that present in patients with celiac disease and in individuals healthy. Patients with type 1 diabetes had inflammatory processes affecting the duodenum.
Hence, the link between a bacterial form and the onset of the disease was hypothesized. The discovery was later published in the Journal of Clinical Endocrinology & Metabolism and could pave the way for understanding alterations of the intestinal system in diabetic patients.
This type of diabetes occurs mainly in young people, even if it can start in adulthood. It is an autoimmune disease, which means that it is caused by the body producing antibodies that destroy its own tissues because they do not recognize them as belonging to the body. The antibodies attack the beta cells inside the pancreas, which produce insulin.
Insulin deficiency prevents the body from using the sugars introduced through food. In this condition, the body produces energy through the metabolism of fats, which involves the production of ketone bodies. Symptoms of lack or lack of insulin include increased urinary volume, sudden weight loss, and an increased sense of thirst.
The triggering factors are heredity, environmental factors, therefore genetic factors, and precisely immune factors, linked to bacterial attacks, and infections. One bacterium, in particular, Mycobacterium avium subspecies paratuberculosis (Map), which mainly affects animals, appears to be related to the onset of type 1 diabetes in Sardinia, Veneto, and the countries of northern Europe.
The bacterium would reach the human body through food, especially milk and dairy products and butchered meats and vegetables that are contaminated and not washed thoroughly. In genetically predisposed individuals, the immune system would be "deceived" by molecular mimicry, exchanging the proteins of one's body for those of the micro bacterium, causing the "autoimmune reaction" which gives rise to inflammation and, in the long run, would favor the onset of diabetes type 1. Studies suggest that Map micro bacterium proteins are similar to those of pancreatic beta cells and that this would promote the autoimmune reaction.
Dr. Antonio Giordano, founder and director of the Sbarro Institute for Cancer Research and Molecular Medicine of the Temple University of Philadelphia and professor of Anatomy and Pathological Histology at the University of Siena.
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